Researchers at the École Polytechnique Fédérale de Lausanne in Switzerland have identified that Turandot proteins can dampen tissue damage caused by autoimmune reactions. The study, published in Current Biology, sheds light on how these molecules modulate immune responses and protect delicate tissues in a living organism.
The team conducted experiments using Drosophila, the common fruit fly, to explore how Turandot proteins influence autoimmunity. Their results show that these proteins can shield insects from autoimmune processes that ordinarily trigger chronic inflammation and tissue injury. While autoimmune diseases in humans, such as arthritis, lupus, and Crohn’s disease, arise when the immune system mistakenly targets the body’s own tissues, the findings in fruit flies offer a window into potential therapeutic strategies that might limit self-damage in similar conditions.
In the study, it was shown that fruit flies produce antimicrobial peptides (AMPs) that are normally aimed at eliminating invading pathogens by disrupting microbial membranes. However, when AMPs are produced in large quantities, they can inadvertently harm the host’s own cells. The Turandot proteins appear to mitigate this risk by altering how cells are recognized during immune challenges, thereby reducing collateral damage while preserving antimicrobial effectiveness.
Mechanistically, Turandot proteins interact with the membranes of host cells, particularly those lining the respiratory epithelium. They cleave phosphatidylserines, molecules that become exposed on stressed cells. This interaction helps healthy cells remain shielded from attack by AMPs during autoimmune episodes, effectively lowering tissue injury without fully compromising pathogen defense.
The researchers propose that similar protective mechanisms could exist in humans. By modulating the interplay between immune effectors and host cell membranes, Turandot-like pathways might be leveraged to limit tissue damage in autoimmune diseases or in settings where an overactive immune response contributes to neurodegenerative injury. The study raises the possibility that enhancing or mimicking this protective system could complement existing therapies and broaden the options available for patients in North America and beyond.
Additionally, the team notes that understanding how Turandot proteins balance antimicrobial defense with cellular protection could inform research into new treatment avenues for neurodegenerative conditions where immune-mediated damage plays a role. While additional work is needed to translate findings from fruit flies to humans, the concept points toward a future where immune modulation helps preserve neuron health and tissue integrity in diseases that share an autoimmune component.